期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 30, 期 1, 页码 98-105出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.01155-09
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资金
- Diabetes and Endocrinology Research Center of the University of Massachusetts [P30-DK52530]
- Howard Hughes Medical Institute
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR021905] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK052530] Funding Source: NIH RePORTER
Bcl2-modifying factor (Bmf) is a member of the BH3-only group of proapoptotic proteins. To test the role of Bmf in vivo, we constructed mice with a series of mutated Bmf alleles that disrupt Bmf expression, prevent Bmf phosphorylation by the c-Jun NH2-terminal kinase (JNK) on Ser(74), or mimic Bmf phosphorylation on Ser(74). We report that the loss of Bmf causes defects in uterovaginal development, including an imperforate vagina and hydrometrocolpos. We also show that the phosphorylation of Bmf on Ser(74) can contribute to a moderate increase in levels of Bmf activity. Studies of compound mutants with the related gene Bim demonstrated that Bim and Bmf exhibit partially redundant functions in vivo. Thus, developmental ablation of interdigital webbing on mouse paws and normal lymphocyte homeostasis require the cooperative activity of Bim and Bmf.
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